Secondary Causes of Hypertension Flashcards

1
Q

primary hyperaldosteronism is from

A

an adrenal adenoma or bilateral adrenal hyperplasia that secretes excess aldosterone see hypertension and hypokalemia and metabolic alkalosis.

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2
Q

why do we not see hypernatremia with primary hyperaldostonism if excess aldosterone should theoretically increase Na, lower K and increase H2O

A

There’s no hypernatremia or edema despite increased renal absorption because of aldosterone escape where increased HTN results in increased blood volume to kidneys so there’s higher GFR and atrial natriuretic peptide so increased Na excretion and no edema that forms

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3
Q

initial evaluation for primary hyperaldosteronism is

A

morning plasma aldosterone concentration (PAC) to plasma renin activity (PRA) ratio.

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4
Q

what is an abnormal PAC/PRA Plasma aldosterone conc / plasma renin activity ratio that would suggest a primary hyperaldosteronism?

A

PAC/PRA ratio >20 with plasma aldosterone >15 ng/dl This isn’t it though. needs a confirmation test

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5
Q

if there’s a positive screening test, what’s the confirmatory test for primary hyperaldosteronism?

A

needs an aldosterone suppression test.

give IV or oral sodium load and measure aldosterone level later and see if it’s suppressed.

If not suppressed then it’s an aldosteronism excess.

This doesn’t rule out if it’s bilateral metaplasia or adrenal adenoma

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6
Q

once primary hyperaldosteronism is confirmed need to figure out if it’s a adrenal adenoma or bilateral adrenal metaplasia and so need

A

CT imaging and look for adrenal gland abnormalities. NOTE CT scan sucks at picking up small tumors and so needs to get a adenal venous sampling

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7
Q

when do you get adrenal venous sampling?

A

when you’ve confirmed that you have primary hyperaldosteronism but CT scan doesn’t tell you if it’s adrenal adenoma or bilateral adrenal hyperplasia

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8
Q

treatment of primary hyperaldosteronism

A

surgery if it’s a single adrenal adenoma medical therapy with spironolactone or eplerone if its bilateral adrenal hyperplasia

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9
Q

what is the pathophysiology for primary hyperaldosteronism and aldosterone escape?

A
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10
Q

if pt has recurrent flash pulmonary edema and atherosclerotic dx and severe hypertension, should think of

A

renovascular dx due to bilateral renal artery stenosis.

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11
Q

Causes of secondary hyperaldosteronism

When the PAC/PRA is not greater than 20

A
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12
Q

features concerning for Renal artery stenosis

A

atherosclerosis in hx, rapid onset of HTN in pts >55 yrs old with risk factors for atherosclerosis (smoking).

Can also see abrupt increase in Cr after being on ACE, recurrent flash pulm edema, abdominal bruits and asymmetrical renal size on imaging.

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13
Q

clinical clues to renovascular disease (chart)

A
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14
Q

treatment for bilateral renal artery stenosis

A

needs ACE i or ARB. no longer contraindicated but most pts will experience a small decline in glomerular filtration rate

HTN in RAS is caused by RAAS which leads to sodium retention and volume expansion. So the ACEi + diuretic will help with prevention of CKD, decrease risk for MI, stroke, decreased mortality.

It’s as effective as angioplasty in pts

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15
Q

in renal artery stenosis who gets stenting?

A

people who fail optimal medical therapy (refractory HTN, inability to tolerate medications, progressive renal insufficiency)

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16
Q

what causes plasma renin levels to be low

what about high?

A

low:

in primary hyperaldosteronism - high aldosterone and so not trying to hold onto water

suppression of antihypertensives- the meds suppress levels

high sodium diet or bilateral renal artery dx - already has high salt water retention so trying not to hold onto water b/c already has HTN

Can be high

if theres renal renovascular hypertension.

17
Q

Pickering Syndrome

A

bilateral renal artery stenosis pts can have flash pulmonary edema despite normal LV EF.

18
Q

how to evaluate for renal artery stenosis?

A

renal doppler ultrasound and CT or MR angiography

19
Q

HTN factors that should make one consider renovascular dx?

A

resistant HTN (uncontrolled despite 3 drug regimen)

malignant HTN (w/ end organ damage)

Onset of severe HTN>180/120 after age 65

severe HTN with diffuse atherosclerosis

recurrent flash pulmonary edema with severe HTN

20
Q

physical exam: asymmetric renal size >1.5 cm, abdominal bruit

lab results: unexplained rise in Cr >30% after starting an ACEi or ARB

imaging results: unexplained atrophic kidney

A

renovascular dx

21
Q

when should spirolactone and eplerenone be stopped prior to screening?

A

Stop 6 weeks prior to screening for primary hyperaldosteronism (aldosterone/renin) because these can affect interpretation of labs.

22
Q

what to do if there’s an incidental adrenloma?

A
23
Q

fibromuscular dysplasia is

A

see twisting and beading of the renal artery. presents with HTN in young female

CT angiography or ultrasound with dopplers is ok to use.

management: ACEi or ARB o r angioplasty

24
Q

hypertension, metabolic alkalosis, hypokalemia

A

think: primary hyperaldosteronism.
testing: stop diuretics to assure euvolumia

get PAC/PRA ratio >20 is positive

confirmatory testing: oral or IV salt loading and fludrocortisone suppresion and captopril challenge tests.